高压氧对大鼠局灶性脑缺血再灌注时神经元特异性烯醇化酶的影响

目的研究高压氧(HBO)对大鼠局灶性脑缺血再灌注(IR)时．大鼠脑梗塞体积．脑组织病理改变及神经元特异性烯醇化酶(NSE)含量的影响。方法用线栓法制备阻断大脑中动脉(MCA)的局灶性脑IR模型。Wistar大鼠30只，随机分为5组：正常对照组(N组n=-6)，缺血再灌注2h 常压空气组(Rt组,n=-6)，缺血再灌注24h 常压空气组(R2组，n=-6)，缺血再灌注2h HBO组(H1组，n=-6)，缺血再灌注24h HBO组(H2组，n=-6)。R1、R2、H1、H2组缺血时间均为2h。R1、R2组暴露于常压空气，H1、H2组暴露于2．5MPa氧气。病理切片用HE染色，用Swanson方法测定脑梗塞体积，用酶联免疫法测定NSE含量。结果H1、H2组与R1、R2组相比，神经元缺血性损害较轻，脑梗塞体积缩小，NSE含量明显下降，差异有统计学意义。结论HBO能减轻缺血性脑损害，保护脑组织。     

普鲁卡因静脉复合麻醉对肝脏血流和氧耗影响的实验研究

采用电磁血流仪和血气分析等技术，研究普鲁卡因静脉复合麻醉对犬体循环血流动力学及肝脏血流和氧耗影响。 １％普鲁卡因复合液以 １．０ｍｇ· ｋｇ－１／ｍｉｎ速度静滴时，随麻醉时间延长，血浆普鲁卡因浓度逐渐升高，６０分钟达５６．９±８．７ｍｇ／Ｌ。体循环各项血流动力学参数趋于稳定，仅在６０分钟产生明显的体循环抑制效应。心率和平均动脉压分别降低２７％、２５％，心指数由３．５２±０．２１Ｌ·ｍｉｎ－１／ｍ２降至 ３． ０８±０．１２Ｌ· ｍｉｎ－１／ｍ２。肝总血流量和氧耗与体循环动力学呈一致性变化。因此，肝脏疾患及肝手术的患者，只要控制血中普鲁卡因浓度不过高，仍可安全实施普鲁卡因静脉复合麻醉。     

Age-related changes in oxygen saturation over the first year of life: A longitudinal study

Stability of oxygen saturation depends on maturation and function of individual components of the respiratory system. The aim of this study was to record and analyse comprehensive oxygen saturation data in a longitudinal study over the first year of life. Detailed sleep studies were performed on 15 normal infants eight times in the first year of life. The accrued oxygen saturation data were analysed on a computerized oximetry data analysis system. Results show the mean sleep saturation levels trending upwards and stabilizing by 185 days. There was an inverse curvilinear relationship between mean age and median desaturation time and the median number of desaturations at ≥95, ≥92 and ≥90% saturation. The mean cumulative desaturation time ≥90% in the first 4 months was 11.08 min (range 2.5–36.57 min). This study demonstrates monotonic patterns of increasing saturation and decreasing number and time of desaturations ≥95% and ≥90% but a random pattern of desaturations ≥85% occurs across the first 6 months of life. Cumulative desaturation times over the first 4 months of life were high and could be important to the development of maturity of the respiratory system. After 6 months, all indices of saturation and desaturation point to a stable and mature respiratory system.     

The onset of ablation of the evoked adductor pollicis muscle twitch in children: a clinical perspective

The time to loss of the adductor pollicis muscle response to ulnar nerve stimulation at 1 Hz (twitch) after succinylcholine, 1.5 mg.kg-1 intravenously (IV), or vecuronium, 0.1 mg.kg-1 (IV), administration was assessed visually in 134 children, age 2-13 yr, during clinically determined, deep halothane, enflurane and isoflurane anaesthesia. The overall time to twitch ablation and duration of succinylcholine's action is in agreement with published times obtained under controlled experimental conditions; the onset time following vecuronium is comparable to those observed during a similar anaesthetic background measured under controlled experimental conditions. Twitch ablation after succinylcholine was achieved in half the time needed following vecuronium regardless of anaesthetic agent. Succinylcholine's and vecuronium's onset time as well as succinylcholine's duration is adequately assessed by the outlined, simple clinical means. The choice of inhalation agent does not affect the time to visible twitch ablation in a clinically relevant manner; nor does it make an appreciable difference, in clinical terms, in succinylcholine's duration of action.     

A developmental role for ataxia-telangiectasia mutated in protecting the embryo from spontaneous and phenytoin-enhanced embryopathies in culture.

Ataxia-telangiectasia (A-T) is characterized by impaired recognition and repair of DNA damage and increased sensitivity to ionizing radiation (IR), cancer, and neurodegeneration. We previously showed pregnant knockout mice lacking the A-T gene product ataxia-telangiectasia mutated (Atm) are highly susceptible to the embryopathic effects of IR, which damages DNA, possibly via generation of reactive oxygen species (ROS). Here we show that Atm more broadly protects against both spontaneous and phenytoin-enhanced embryopathies. In the absence of drug exposure, cultured embryos from pregnant Atm knockout mice showed more embryopathies than wild-type littermates, with a gene dose-dependent decrease in susceptibility from -/- to +/- to +/+ embryos (p < 0.05). A similar but significantly enhanced gene dose-dependent pattern of embryopathic susceptibility was evident in Atm knockout embryos exposed to the ROS-initiating teratogen phenytoin (p < 0.05). These results provide the first evidence that Atm has a broad developmental importance beyond IR embryopathies, possibly by protecting the embryo from constitutive and xenobiotic-enhanced oxidative stress, with even heterozygotes showing increased risk. This developmental role of Atm further implicates DNA damage in ROS-mediated teratogenesis and DNA damage response and repair as risk factors for individual susceptibility.     

肝移植术后肝动脉血栓形成的治疗方法探讨

目的探讨肝移植术后肝动脉血栓形成的治疗方法。方法回顾性分析我院自2001年11月至2005年1月收治肝移植术后肝动脉血栓形成患者14例,分别采用动脉溶栓、血管支架植入、高压氧治疗及再次肝移植治疗。结果动脉溶栓11例,成功率45.5%(5/11),2例随访12个月肝功能正常,另3例均于随访期死亡,其中2例因吻合口狭窄曾行血管支架植入术。高压氧治疗3例,随访7个月,临床效果较好。急诊再次肝移植2例,术后均死于多器官功能衰竭。结论肝移植术后肝动脉血栓形成,动脉溶栓及血管支架植入治疗存在局限性,高压氧治疗效果良好,可与其他保守治疗联合使用,应避免急诊再次肝移植。     

高压氧在手外科创伤中的应用

目的探讨高压氧在手外科常见创伤中的应用与临床效果。方法2002年3月～2005年12月对手外科常见创伤:断指再植术后血管危象、肢体顽固性溃疡、手部骨折、肢体压砸伤等按常规治疗组和高压氧治疗组进行观察。结果断指再植术后血管危象常规治疗组和高压氧治疗组无明显差异(t检验,P>0.05);肢体顽固性溃疡、手部骨折、肢体压砸伤等的常规治疗组和高压氧治疗组差异有显著性(t检验,P<0.05)。结论高压氧在手外科常见创伤中合理选择应用,可以取得较好的临床效果。     

弱激光血疗法的发展及展望

本文主要介绍了弱激光血疗的机制及其在我国的发展过程.弱激光血疗法起源于前苏联的紫外光量子疗法,传入我国后经历了静脉内照射疗法,离体血液激光照射回输疗法,口咽部照射伴吸氧疗法,鼻腔内照射疗法等.本文对各种疗法的特点及临床应用进行了详细叙述.有些学者认为,中医的观点也能揭示激光血疗的机制.从中医辨证的角度,人的体质分为虚证和实证.结合中医针灸的虚则补之,实则泻之的原理,根据患者的虚实状况,采用含有中医补泻信息的调制激光照射血液,同时加照相关敏感穴位,促进疗效,以体现中医的辨证施治的原则可取得更好的疗效.     

Pathogenesis of progressive muscular dystrophy: studies on free radical metabolism in an animal model

Evidence to suggest the presence of abnormal metabolism of oxygen free radicals in progressive muscular dystrophy is presented using an animal model. In the superficial pectoral muscles of dystrophic chickens, enzyme activities regulating the metabolism of oxygen free radicals, i.e., catalase, superoxide dismutases and glutathione peroxidase, were significantly elevated within 1 week of hatching. Activities of related enzymes, i.e., glutathione reductase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase were also elevated. In contrast, the specific activity of phosphofructokinase, the rate-limiting enzyme of the glycolytic pathway, was normal during the first 4-week period. These results suggest that there is an increased turnover of oxygen free radicals in the dystrophic muscle. This concept appears important in a further investigation of the pathogenesis and treatment of progressive muscular dystrophies.     

The superoxide anion may mediate short- but not long-term effects of ultraviolet radiation on melanogenesis

Abstract The present study was carried out to examine the role of reactive oxygen species in mediating the melanogenic effects of UVR. B16 mouse melanoma cells responded to a single dose of UVR by showing increases in their melanin content. Although there was a small increase in melanin at 48-72 hours, which was associated with a rise in tyrosinase activity at 48 h, the greatest change occurred at 3 h and this was not associated with an increase in tyrosinase activity. This short-term response, unlike the more delayed melanogenic response, was reduced by superoxide dismut-ase (SOD). Xanthine oxidase (XO), which generates the superoxide anion (O₂). also increased the melanin content of B16 melanoma cells with effects at 3 h and 48 h. As with UVR, the delayed response was accompanied by an increase in tyrosinase activity but no such association was evident at 3 h. In addition, the short-term effect, like that seen with UVR, was reduced with SOD and to a lesser extent with catalase. In contrast to the effects found with XO, glucose oxidase, which generates hydrogen peroxide, had no effect on the melanin content or tyrosinase activity of the B16 cells. These results confirm previous observations that UVR is able to act directly on cells to bring about delayed increases in melanogenesis. They further demonstrate that UVR also stimulates melanogenesis through a more rapid action that is not associated with an activation of tyrosinase. This effect could be mediated by the O₂ which, rather than activating tyrosinase, could act by serving as a substrate for the enzyme.